Structural heart disease Flashcards

1
Q

what are structural heart diseases and what are the types

A

Defects effective valves and chambers of the heart

1) congenital
2) later in life

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2
Q

what are the congenital structural heart diseases

A
atrial septal defects 
ventricular septal defect 
coarctation of aorta 
patent foramen ovale 
patent ductus arteriosus 
tetralogy of Fallot
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3
Q

what is the pathology of ventricular septal defect? Symptoms? treatments?

A

Ventricular septal defect : walls between 2 ventricles fails to develop normally → hole in the wall → mixing of blood in L and R ventricles
Symptoms: poor weight gain , decreased appetite, palpitations
Sometimes the hole will close as the child grows
Correction : open heart surgery / cardiac catheterisation

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4
Q

what is the tetralogy of fellow and how is it treated

A

Tetralogy of fellow ( 4 diseases together )
Ventricular septal defect
Pulmonary stenosis ( pulmonary trunk is narrow
Widening of aortic wall ( allows back flow of blood from ventricle to aorta
Right ventricle hypertrophy ( thickening of right ventricle wall)
Treatment: surgery

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5
Q

what is atrial septal defect

A

Atrial septal defect : hole in the wall between the 2 atria due to abnormal development

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6
Q

what is coaction of the aorta

A

Coarctation of aorta : narrowing of wall of the artery → means ventricle must work harder to push blood → thickening of ventricle → heart failure

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7
Q

what are the 2 types of structural valvular defects

A

These can be divided into 2
stenotic lesions: narrowing
Hardening of the valve reduces the responsiveness to ventricular systolic pressure, thus during ventricular contraction a greater contractile force is required to force the valve to open
regurgitation lesions: dilations
left sided valvular lesions are more clinically significant: mitral stenosis and aortic stenosis

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8
Q

what is aortic stenosis? what is it’s pathophysiology and complications

A

narrowing of aortic valve
Pathology
mechanical stress ( ie abnormal blood flow) damages endocardium leading to proximal fibrosis and calcification;
valvular endocardium is damaged which initiates an inflammatory process leading to calcium deposition + fibrosis , limiting leaflet mobility → stenosis + less systemic blood flow
In Rheumatic disease : autoimmune inflammatory reaction triggered by prior strep infection that targets valvular endothelium → inflammation + calcification

Complications
Long-standing pressure overload → left ventricular hypertrophy (LVH).
Ventricle maintains normal wall stress (afterload) despite the pressure overload produced by stenosis
As the stenosis worsens, the adaptive mechanism ( LVH) fails and left ventricular wall stress increases.
Systolic function declines as wall stress increases, with resultant systolic heart failure.

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9
Q

what are the causes and risk factors of aortic stenosis

A
Risk factors : 
Hypertension 
LDL 
Smoking 
High C peptide 
Congenital bicuspid valves
CKD ( chronic kidney disease) 
Due to more infection 
Radiotherapy 
Due to cancer 
Older age 
Due to calcification 
Causes: 
Rheumatic heart disease 
Most common cause in developing countries 
Congenital heart disease 
Calcium build up 

Preceded by aortic sclerosis ( aortic valve thickening w/o flow limitation)

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10
Q

what is the presentation of someone with AS

A
History and presentation 
Exertional dyspnoea and fatigue
Chest pain
Shrill Ejection systolic murmur (≥3/6 is present with a crescendo-decrescendo pattern that peaks in mid-systole and radiates to the carotid)
Confirmed by echocardiography ( look for LV hypertrophy and thickening) 
H/O  ( history of) Rheumatic fever
high lipoprotein
high LDL, CKD
age >65
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11
Q

what is the management for AS

A

Management
(Aortic Valve replacement) (AVR)
The primary treatment of symptomatic AS
Asymptomatic patients with severe AS who have an LVEF <50% or who are undergoing other cardiac surgery.
AVR may be considered in asymptomatic patients with very severe AS or severe AS with rapid progression, an abnormal exercise test, or elevated serum B-type natriuretic peptide (BNP) levels

Medications 
Balloon aortic valvuloplasty
Antihypertensive
 ACE inhibitors
Statins
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12
Q

what are investigations for aortic stenosis

A
Investigations : 
ECG ( for regurgitation only) 
Transthoracic echocardiography 
Chest x ray  ( for LV hypertrophy) 
Cardiac catheterisation 
Cardiac MRI / CT scan
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13
Q

what is mitral stenosis? what is it’s pathophysiology and complications

A

structural deformity of mitral valve reducing left ventricular inflow

Pathophysiology
Obstruction to left ventricular inflow at the level of mitral valve due to structural abnormality of the mitral valve
Acute insult lead to formation of multiple foci + infiltrated in the edno + myocardium along walls of valves
With passage of time → thickens → calcified → stenosis

Complications
Initially moderate exercise or tachycardia → exertional dyspnoea due to increased left atrial pressure

Severe mitral stenosis → increase in left atrial pressure
Lead to transudation of fluid into the lung interstitium
Leads to dyspnoea at rest or exertion
Pulmonary hypertension may develop as the result of it

The restricted orifice limits filling of left ventricle limiting cardiac output → can lead to right heart failure

Hemoptysis if bronchial vein rupture

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14
Q

what are the causes and risk factors of mitral stenosis

A
Causes: 
Rheumatic fever 
Main cause in developing countries 
Typically disease occurs decades after infection 
Carcinoid syndrome 
Ergot / serotonergic drugs 
SLE 
Mitral annular calcification due to aging 
Amyloid 
Rheumatoid arthritis 
Whipple disease 
Congenital deformity
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15
Q

What is the presentation of someone with mitral stenosis

A
Presentation:
H/0 of Rheumatic fever
Dyspnoea
orthopnoea
Diastolic murmur
Loud P2
Neck vein distention
Hemoptysis
40-50 years age
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16
Q

what is the management of mitral stenosis

A

Management
Progressive asymptomatic
No therapy required

Severe asymptomatic
no therapy generally required adjuvant balloon valvotomy

Severe symptomatic
diuretic, balloon valvotomy, valve replacement & repair adjunct b blockers

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17
Q

what are the investigations of mitral stenosis

A
Investigations 
ECG 
Transthoracic echocardiography
Chest X ray 
Cardiac catheterisation
Cardiac MRI/CT Scan
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18
Q

what is aortic regurgitation ? pathology ? Complications?

A

diastolic leakage of blood from aorta → left ventricle

Pathologies
Incompetence of valve leaflets due to:
Intrinsic valve disease
Dilation of aortic root
Can be :
Chronic : → fulminate into congestive cardiac failure
Acute → medical emergency presenting with sudden onset of pulmonary oedema and hypotension or cardiogenic shock

Complications 
Acute AR : 
Increase blood volume in LV during systole
LV end diastolic pressure increases 
increase in pulmonary venous pressure 
dyspnea and pulmonary oedema
heart failure cardiogenic shock

Chronic AR
gradually increase in LV volume
LV enlargement and eccentric hypertrophy
Early stages: Ejection fraction normal or slightly increase
After some time: Ejection fraction falls and LV end systolic volume rises
Eventually LV dyspnoea lower coronary perfusion ischemia, necrosis and apoptosis → heart failure

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19
Q

how does rheumatic fever effect the heart

A

antibodies against rheumatic fever have a similar shape to heart muscle antigens and so will bind

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20
Q

how does infective endocarditis cause heart disease

A

Causes vegetations of valve cusps leading to inadequate closure and leads to rupture of leaflets/paravalvular leaks

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21
Q

What are the causes and risk factors of aortic regurgitation

A

Congenital + acquired
Rheumatic heart disease / rheumatic fever (acute + chronic AR)
Infective endocarditis (Acute AR ) ( Causes vegetations of valve cusps leading to inadequate closure and leads to rupture of leaflets/paravalvular leaks.)
Aortic valve stenosis
Congenital heart defects
bicuspid aortic valves (chronic AR)
Chest trauma ( cause tear in aorta)

Aortic root dilation : 
Connective tissue disease / collagen vascular diseases 
 marfan syndrome
Idiopathic 
Ankylosing spondylitis 
Traumatic 

Risk factors
high bp, systemic hypertension

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22
Q

what is the presentation of aortic regurgitation

A
Acute AR
Cardiogenic shock
Tachycardia
Cyanosis
Pulmonary edema
Austin flint murmur
Chronic AR
Wide pulse pressure
Corrigan (wide hammer pulse)
Aka forceful pulse that suddenly collapses
Pistol shot pulse (Traube sign)
Loud cracking sound heard over the stethoscope due to dilation and collapse of aorta
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23
Q

what is the management of aortic regurgitation

A

Management

Prevention first !: treat rheumatic fever and infective endocarditis

Acute ARI:
Inotropes/vasodilators & valve replacement & repair
See valves replacement in aortic stenosis

Chronic asymptomatic
If LV function is normal can be managed by drugs or reassurance

Chronic symptomatic
First line is valve replacement with adjunct vasodilator therapy

24
Q

what investigations would you carry out for aortic stenosis

A
Investigations 
Transthoracic echocardiography
Chest X ray 
Cardiac catheterisation
Cardiac MRI/CT Scan
25
Q

what is mitral regurgitation ? pathophysiology? complications

A

: backflow of blood from L ventricle to aorta during systole

Pathophysiology
Infectious endocarditis leads to abscess formation, vegetations, rupture of chordae tendineae and leaflet perforation

Complications
Chronic MR
progression leads to eccentric hypertrophy
leading to elongation of myocardial fibres
Increases left end diastolic volume
Increase in preload & a decrease in afterload
Increase in end- diastolic volume and a decrease in end-systolic volume
Eventually prolonged volume overload leads to left ventricular dysfunction and increased left ventricular end-systolic diameter
Can lead to heart failure

26
Q

causes of mitral regurgitation

A
Causes 
Acute : 
Mitral valve prolapse 
Rheumatic heart disease 
Infective endocarditis 
Following valvular surgery 
Prosthetic mitral valve dysfunction
Chronic: 
Rheumatic heart disease
SLE
Scleroderma 
Hypertrophic cardiomyopathy 
Drug related
27
Q

presentation of mitral regurgitation

A
Presentation:
Dyspnea                        
diminished S1, murmur high pitched , blowing sound 
Fatigue                              
Orthopnea
Chest pain 
Atrial fibrillation 
Due to backflow of blood into left atrium
28
Q

management of mitral regurgitations

A

Management
Acute MR
Emergency Surgery adjunct preoperative diuretics adjunct intra-aortic balloon counterpulsation

Chronic asymptomatic
1st ACE inhibitors or Beta blockers
If left ventricular ejection fraction is less than 60% 1st line is surgery

Chronic symptomatic
1st surgery plus medical treatment
If left ventricular ejection fraction is less than 30% 1st line is Intra-aortic balloon counterpulsation

29
Q

Investigations of mitral regurgitations

A
ECG
Transthoracic echocardiography
Chest X ray 
Cardiac catheterisation
Cardiac MRI/CT Scan
30
Q

what is Cardiomyopathies and what are the 3 types

A

Disease of heart muscle making it harder to pump blood to rest of body
Can lead to heart failure
3 main types :
dilated , hypertrophic , restrictive

31
Q

what is dilated cardiomyopathy pathophysiology ? complications

A

Pathophysiology
Ventricular chamber enlargement + systolic dysfunction with normal LV wall thickness

Complications
Enlargement of the left ventricle
↓ejection fraction , ↑ ventricular wall stress, ↑ end systolic volumes.
Due to Left ventricle not able to contract fully

Early compensatory mechanisms
↑ heart rate and tone of the peripheral vascular system.
Due to neurohumoral activation of the renin-angiotensin aldosterone system → ↑ circulating levels of catecholamines.
↑ levels of natriuretic peptides
Help increase contraction
Eventually these compensatory mechanisms become overwhelmed and the heart fails.

32
Q

causes of dilated cardiomyopathy

A
Primary  25% 
Idiopathic (without family history) 
Familial 
Rare autosomal dominant inheritance patterns 
Secondary 
Heart valve disease
After childbirth 
Thyroid disease 
Myocarditis 
Alcoholism 
Autoimmune disorders
Ingestion of drugs 
Mitochondrial disorders
33
Q

Presentation of dilated cardiomyopathy

A
Dyspnoea,                 
displaced apex beat, S3 or systolic murmur
fatigue, 
angina, 
pulmonary congestion
low cardiac output
34
Q

management of dilated cardiomyopathy

A

1) diet modifications ie fluid restriction
2) treatment of underlying problems
3) treating symptoms of heart failure ie ACE / B blockers w / wo diuretics –> if medication ineffective move onto surgery
4) Treatment for arrhinias
5) anticoagulants for thrombolytic events

see google docs please

35
Q

Investigations of dilated cardiomyopathy

A
Investigations:
Genetic Testing
Viral serology
Rule out infection 
ECG
Chest X ray 
Cardiac catheterisation
Cardiac MRI/CT Scan
Exercise stress test 
Echocardiograph
36
Q

what is the hallmark finding of dilated cardiomyopathy

A

Hallmark finding : In autopsy LV dilation > 4mm

37
Q

what is hypertrophic cardiomyopathy ? pathophysiologies ? complications

A

Pathophysiology
Increase in LV wall thickness ( hypertrophy) that is inappropriate, often asymmetrical + occurs in absence of hypertrophy stimulus
LV hypertrophy often occurs in interventricular septum
→ obstruction of flow through the LV outflow tract

Complication
Most patients with HCM have abnormal diastolic function,
impairs ventricular filling ↑ filling pressure, despite a normal or small ventricular cavity.
These patients have abnormal calcium kinetics and subendocardial ischemia, which are related to the profound hypertrophy and myopathic process.

38
Q

Causes of HCM

A

Familial

Autosomal dominant Mendelian inherited disease

39
Q

Presentation of HCM

A

Presentation
Most patents are asymptomatic . Usual first clinical manifestation is sudden death due to ventricular tachycardia / fibrillation

Sudden cardiac death   
Double carotid artery impulse, S3 gallop,
Syncope                          
ejection systolic murmur
Presyncope
Congestive heart failure
Dizziness
Palpitations
Angina
40
Q

Management of HCM

A

HCM with symptoms :
B blockers –> verapamil if B blockers don’t work

add disopyramide
surgery if all else fails

Please see insendi

41
Q

Investigations of HCM

A

Investigations
Hemoglobin level: Anemia exacerbates chest pain and dyspnea
Brain natriuretic peptide (BNP)
troponin T levels: Elevated BNP, NT-proBNP, and troponin T levels are associated with a higher risk of cardiovascular events, heart failure, and death
Echocardiography
Chest Xray
Cardiac MRI

42
Q

what is restrictive cardiomyopathy? Pathophysiology? complications?

A

Pathophysiology
Increased stiffness of myocardium :
Infiltrative cardiomopathies due to deposition of abnormal substances ie, amyloid proteins, noncaseating granulomas, iron) within the heart tissue.
→ stiffening of ventricular walls → leading to diastolic dysfunction.

Restrictive physiology predominates in the early stages:
causing conduction abnormalities and diastolic heart failure.
Normal systolic function
Adverse remodelling may lead to systolic dysfunction and ventricular arrhythmias in advanced cases.

Complications
Increased stiffness of the myocardium → ↑ ventricular pressures with small increases in volume.
Thus, accentuated filling occurs in early diastole and terminates abruptly at the end of the rapid filling phase.

Patients typically have:
↓compliance ( ↑ diastolic stiffness),
Inadequate left ventricle filling at normal pressure → ↓cardiac output.
Atrial enlargement due to impaired ventricular filling during diastole but volume + thickness of ventricles are normal

43
Q

what are causes of restrictive cardiomyopathies

A

Causes
Primary causes
Idiopathic
familial (has been related to troponin I or desmin mutations, the latter often in association with a skeletal myopathy)

various systemic disorders/ secondary causes :

ie haemochromatosis
 Amyloidosis
Sarcoidosis
Fabry's disease
carcinoid syndrome
Scleroderma
anthracycline toxicity
previous radiation.
44
Q

what are presentations of restrictive cardiomyopathies

A
Presentation 
comfortable in the sitting position
Due to fluid in the abdomen or lungs
Frequently have ascites and pitting edema of the lower extremities
Due to fluid not being pumped property 
Enlarged liver 
Due to fluid 
Can be painful
Weight loss 
cardiac cachexia 
↑ jugular venous pressure 
↓ pulse volume is decreased
consistent with decreased stroke volume and cardiac output.
Amyloidosis symptoms 
Easy bruising
periorbital purpura
Macroglossia
systemic findings: 
carpal tunnel syndrome,
45
Q

Management of RCM

A

Management

Heart failure medication
Guideline-directed medical therapy for heart failure, including angiotensin-converting enzyme inhibitors or angiotensin receptor II blockers, diuretics and aldosterone inhibitors should be initiated in patients with reduced LV

Antiarrhythmic Therapy

Immunosuppression
Steroids ( for amyloidosis or other immune problems) 

Pacemaker

Cardiac transplantation

46
Q

investigations of RCM

A
Investigations 
CBC
Serology
Amyloidosis check
Chest Xray
ECG
Echocardiography
Catheterisation
MRI/Biopsy
47
Q

Look at tutorial

A

on google docs

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